Resumo:
Helicobacter pylori infection is a significant risk factor for the development of inflammatory
and neoplasic changes in the stomach, contributing to the pathogenesis of gastric diseases,
particularly through epigenetic mechanisms. This experimental study aimed to examine the
DNA methylation profile of the IL6, SOCS1, MGMT, and MLH1 genes in gastric mucosal
samples, considering the presence of H. pylori infection and the detection of the virulence
gene cagA. Samples underwent DNA extraction, followed by sodium bisulfite conversion
and analysis using the MS-HRM technique. IL6 methylation was categorized into 0-25% and
25-50%, with stratification by sex, age, and bacterial strain status. Statistical analyses
included the Student’s t-test to compare mean methylation levels between H. pylori-positive
and -negative groups, and chi-square or Fisher’s exact test, as appropriate, considering p <
0,05 as the significance threshold for associations between categorical variables. The results
indicated that infected individual were twice as likely to exhibit moderate methylation of the
IL6 gene compared to non-infected individuals (OR = 2.00; 95% CI: 0.56–7.62; p = 0.284),
and those infected with cagA-positive strains had a higher risk compared to those with cagA-
negative strains (OR = 1.56; 95% CI: 0.41–5.85; p = 0.508), although these differences were
not statistically significant. Among men, a significant association was observed (p = 0.035),
with 100% of infected individuals showing moderate methylation versus 40% in the non-
infected group; no significant difference was found among women (p = 0.765). Methylation
of the SOCS1 and MLH1 genes was not detected in any of the samples, regardless of
infection status, while MGMT methylation was observed in only three individuals (6.82%),
all at low levels, preventing statistical analysis. Although no statistically significant
association was observed with cagA status, all men infected with cagA-positive strains
exhibited moderate methylation. These findings suggest that H. pylori infection may
modulate IL6 gene methylation, particularly in males, and underscore the role of epigenetic
mechanisms in the molecular pathways underlying gastric inflammation and disease
progression, especially in high- prevalence populations.
